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Rattus norvegicus

ABSTRACT: Mechanisms of variable ventilation in experimental lung injury

PROVIDER: PRJNA312344 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3175220.fastq.gz	Fastqsanger.gz
	SRR3175230.fastq.gz	Fastqsanger.gz
	SRR3175240.fastq.gz	Fastqsanger.gz
	SRR3175250.fastq.gz	Fastqsanger.gz
	SRR3175260.fastq.gz	Fastqsanger.gz

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Rattus norvegicus

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Project description:Open lung approach with low tidal volume mechanical ventilation attenuates lung injury in rats with massive brain damage

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MAP Kinase Phosphatase-1 Modulates Regional Effects of Injurious Mechanical Ventilation in Rodent Lungs

Project description:Scientific knowledge on the subjects: Injurious mechanical ventilation amplifies acute lung injury in a heterogeneous and regional fashion but the molecular mechanisms underlying regional lung injury and the protective effects of prone positioning are unclear. Regionally injurious ventilation is associated with discrete differential lung transcriptomic changes. Ventilating in the prone, compared with the supine position abrogates regional injury by depressing MKP-1. Adult rats were ventilated with high (18 mL/Kg, PEEP 0) tidal volume (Vt) in supine or prone position. Non ventilated rats were used as controls. Dorsal-caudal lung mRNA was analyzed by microarray.

2011-08-26 | E-GEOD-31678 | biostudies-arrayexpress

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Project description:Molecular Signatures of Trauma Hemorrhagic Shock-Induced Lung Injury: Hemorrhage- and Injury-Associated Genes

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Project description:In the present study we seek to identify changes in lung gene expression under mechanical ventilation in uninjured as well as acutely and chronically injured lungs. A standard volume-controlled lung-protective ventilatory protocol is compared to a concept of mechanical ventilation using variable tidal volumes.

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Project description:Gene Expression Changes due to Rat Lung Ischemia-Reperfusion Injury

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Ventilator-induced lung injury in wild-type and jnk1 knockout mice

Project description:Background: Mechanical ventilation causes ventilator-induced lung injury in animals and humans. Mitogen-activated protein kinases have been implicated in ventilator-induced lung injury though their functional significance remains incomplete. We characterize the role of p38 mitogen-activated protein kinase/ mitogen activated protein kinase kinase-3 and c-Jun-NH2-terminal kinase-1 in ventilator-induced lung injury and investigate novel independent mechanisms contributing to lung injury during mechanical ventilation. Methodology and Principle Findings: C57/BL6 wild-type mice and mice genetically deleted for mitogen-activated protein kinase kinase-3 (mkk-3-/-) or c-Jun-NH2-terminal kinase-1 (jnk1-/-) were ventilated, and lung injury parameters were assessed. We demonstrate that mkk3-/- or jnk1-/- mice displayed significantly reduced inflammatory lung injury and apoptosis relative to wild-type mice. Since jnk1-/- mice were highly resistant to ventilator-induced lung injury, we performed comprehensive gene expression profiling of ventilated wild-type or jnk1-/- mice to identify novel candidate genes which may play critical roles in the pathogenesis of ventilator-induced lung injury. Microarray analysis revealed many novel genes differentially expressed by ventilation including matrix metalloproteinase-8 (MMP8) and GADD45a. Functional characterization of MMP8 revealed that mmp8-/- mice were sensitized to ventilator-induced lung injury with increased lung vascular permeability. Conclusions: We demonstrate that mitogen-activated protein kinase pathways mediate inflammatory lung injury during ventilator-induced lung injury. C-Jun-NH2-terminal kinase was also involved in alveolo-capillary leakage and edema formation, whereas MMP8 inhibited alveolo-capillary protein leakage. Keywords: response to injury, genetically modified mouse

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MiRNA profiling in Rattus norvegicus pancreatic cells

Project description:This SuperSeries is composed of the SubSeries listed below.

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Expression data from intact and ventilation-preconditioned murine lungs

Project description:To study the effects of previous exposure to mechanical ventilation may modify the development of Ventilator-induced lung injury, preconditioning was induced by low-pressure ventilation for 90 minutes. After 1 week, intact (sham) and preconditioned mice were sacrificed, the lungs extracted and gene expression measured in order to identify differences responsible for the observed tolerance to ventilator-induced lung injury observed in preconditioned animals. 6 samples were analyzed, from 3 intact (sham) and 3 preconditioned CD1 mice.

2015-08-21 | E-GEOD-65783 | biostudies-arrayexpress

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